The induction of chromosome-type aberrations in G1 by methyl methanesulfonate and 4-nitroquinoline-N,-oxide, and the non-requirement of an S-phase for their production.
Human lymphocytes were treated in G1 with 4-nitroquinoline-N-oxide (4NQO) and methyl methanesulfonate (MMS) and then incubated in the presence or absence of cytosine arabinoside (ara-C). There was an increase in aberration frequency in those cells incubated with ara-C compared with those treated with 4NQO or MMS alone. This increase was restricted to chromosome-type aberrations. When cells were treated in G2 with 4NQO and then incubated with ara-C until fixation, there was an increase in deletions compared with cells treated with 4NQO alone. No exchange aberrations were observed following any treatment even when deletion frequencies were high, as in the case with 4NQO plus ara-C treatment. These results suggest that ara-C can inhibit the repair of DNA damage induced by 4NQO and MMS that is converted into aberrations. They also show that the terms "S-dependent' and "S-independent' used to describe the modes of action of chemical clastogens are not valid.
D015112:4-Nitroquinoline-1-oxide / Q000494:pharmacology; D002478:Cells, Cultured; D002869:Chromosome Aberrations; D002875:Chromosomes / Q000187:drug effects*; D003561:Cytarabine / Q000494:pharmacology; D004359:Drug Therapy, Combination; D006801:Humans; D007399:Interphase; D008214:Lymphocytes / Q000648:ultrastructure; D008741:Methyl Methanesulfonate / Q000494:pharmacology; D009153:Mutagens
D009153:Mutagens; D003561:Cytarabine; D015112:4-Nitroquinoline-1-oxide; D008741:Methyl Methanesulfonate